title: Dietary glycine blunts liver injury after bile duct ligation in rats.
abstract: OBJECTIVE
  To investigate the effects of (dietary) glycine against oxidant-induced injury caused by bile duct ligation (BDL).
  
  
  METHODS
  Either a diet containing 5% glycine or a standard diet was fed to male Sprague-Dawley (SD) rats. Three days later, BDL or sham-operation was performed. Rats were sacrificed 1 to 3 d after BDL. The influence of deoxycholic acid (DCA) in the presence or absence of glycine on liver cells was determined by measurement of calcium and chloride influx in cultivated Kupffer cells and lactate dehydrogenase (LDH) activity was determined in the supernatant of cultivated hepatocytes.
  
  
  RESULTS
  Serum alanine transaminase levels increased to about 600 U/L 1 d after BDL. However, enzyme release was blunted by about two third in rats receiving glycine. Release of the alkaline phosphatase and aspartate aminotransferase was also blocked significantly in the group fed glycine. Focal necrosis was observed 2 d after BDL. Glycine partially blocked the histopathological changes. Incubation of Kupffer cells with DCA led to increased intracellular calcium that could be blocked by incubation with glycine. However, systemic blockage of Kupffer cells with gadolinium chloride had no effects on transaminase release. Incubation of isolated hepatocytes with DCA led to a significant release of LDH after 4 h. This release was largely blocked when incubation with glycine was performed.
  
  
  CONCLUSIONS
  These data indicate that glycine significantly decreased liver injury, most likely by a direct effect on hepatocytes. Kupffer cells do not appear to play an important role in the pathological changes caused by cholestasis.
authors.affiliation: Department of Internal Medicine I, University of Regensburg, Regensburg 93042, Germany. froh.science@mac.com.
authors.forename: Matthias
authors.initials: M
authors.lastname: Froh
authors.forename: Zhi
authors.initials: Z
authors.lastname: Zhong
authors.forename: Peter
authors.initials: P
authors.lastname: Walbrun
authors.forename: Mark
authors.initials: M
authors.lastname: Lehnert
authors.forename: Susanne
authors.initials: S
authors.lastname: Netter
authors.forename: Reiner
authors.initials: R
authors.lastname: Wiest
authors.forename: Lars
authors.initials: L
authors.lastname: Conzelmann
authors.forename: Erwin
authors.initials: E
authors.lastname: Gabele
authors.forename: Claus
authors.initials: C
authors.lastname: Hellerbrand
authors.forename: Jurgen
authors.initials: J
authors.lastname: Scholmerich
authors.forename: Ronald-G
authors.initials: RG
authors.lastname: Thurman
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D002712:Chlorides / Q000378:metabolism; D002756:Cholagogues and Choleretics / Q000494:pharmacology; D002779:Cholestasis / Q000150:complications* / Q000209:etiology*; D003840:Deoxycholic Acid / Q000494:pharmacology; D004032:Diet; D004195:Disease Models, Animal; D005998:Glycine / Q000008:administration & dosage / Q000627:therapeutic use*; D018684:Glycine Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007728:Kupffer Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008026:Ligation / Q000009:adverse effects; D008107:Liver Diseases / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002712:Chlorides; D002756:Cholagogues and Choleretics; D018684:Glycine Agents; D003840:Deoxycholic Acid; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D002118:Calcium; D005998:Glycine